Han Li-Yuan, Liu Kui, Lin Xia-Lu, Zou Bao-Bo, Zhao Jin-Shun
Department of Preventive Medicine, Zhejiang Provincial Key Laboratory of Pathological and Physiological Technology, Medical School of Ningbo University, Ningbo, China E-mail :
Asian Pac J Cancer Prev. 2014;15(15):6131-6. doi: 10.7314/apjcp.2014.15.15.6131.
Epidemiology studies have reported conflicting results between glutathione S-transferase Mu-1 (GSTM1), glutathione S-transferase theta-1 (GSTT1) and glutathione S-transferase pi-1 (GSTP1) and ovarian cancer (OC) susceptibility. In this study, an updated meta-analysis was applied to determine whether the deletion of GSTM1, GSTT1 and GSTP1 has an influence on OC susceptibility.
A published literature search was performed through PubMed, Embase, Cochrane Library, and Science Citation Index Expanded database for articles published in English. Pooled odds ratios (ORs) and 95% confidence intervals (95%CIs) were calculated using random or fixed effects models. Heterogeneity between studies was assessed using the Cochrane Q test and I2 statistics. Sub-group analysis was conducted to explore the sources of heterogeneity. Sensitivity analysis was employed to evaluate the respective influence of each study on the overall estimate.
In total, 10 published studies were included in the final analysis. The combined analysis revealed that there was no significant association between GSTM1 null genotype and OC risk (OR=1.01, 95%CI: 0.91-1.12). Additionally, there was no significant association between GSTT1 genetic polymorphisms and OC risk (OR=0.98, 95% CI: 0.85-1.13). Similalry, no significant associations were found concerning the GSTP1 rs1695 locus and OC risk. Meanwhile, subgroup analysis did not show a significant increase in eligible studies with low heterogeneity. However, sensitivity analysis, publication bias and cumulative analysis demonstrated the reliability and stability of the current meta-analysis.
These findings suggest that GSTs genetic polymorphisms may not contribute to OC susceptibility. Large epidemiological studies with the combination of GSTM1 null, GSTT1 null and GSTP1 Ile105Val polymorphisms and more specific histological subtypes of OC are needed to prove our findings.
流行病学研究报告了谷胱甘肽S-转移酶Mu-1(GSTM1)、谷胱甘肽S-转移酶Theta-1(GSTT1)和谷胱甘肽S-转移酶Pi-1(GSTP1)与卵巢癌(OC)易感性之间存在相互矛盾的结果。在本研究中,应用更新的荟萃分析来确定GSTM1、GSTT1和GSTP1的缺失是否对OC易感性有影响。
通过PubMed、Embase、Cochrane图书馆和科学引文索引扩展数据库对以英文发表的文章进行已发表文献检索。使用随机或固定效应模型计算合并比值比(OR)和95%置信区间(95%CI)。使用Cochrane Q检验和I²统计量评估研究之间的异质性。进行亚组分析以探索异质性的来源。采用敏感性分析来评估每项研究对总体估计的各自影响。
最终分析共纳入10项已发表研究。合并分析显示,GSTM1无效基因型与OC风险之间无显著关联(OR = 1.01,95%CI:0.91 - 1.12)。此外,GSTT1基因多态性与OC风险之间无显著关联(OR = 0.98,95%CI:0.85 - 1.13)。同样,未发现GSTP1 rs1695位点与OC风险之间存在显著关联。同时,亚组分析未显示低异质性的合格研究有显著增加。然而,敏感性分析、发表偏倚和累积分析证明了当前荟萃分析的可靠性和稳定性。
这些发现表明,谷胱甘肽S-转移酶基因多态性可能与OC易感性无关。需要进行结合GSTM1无效、GSTT1无效和GSTP1 Ile105Val多态性以及更具体的OC组织学亚型的大型流行病学研究来证实我们的发现。